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International Immunology Advance Access originally published online on November 1, 2004
International Immunology 2004 16(12):1789-1798; doi:10.1093/intimm/dxh180
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© 2004 The Japanese Society for Immunology

Altered splenic B cell subset development in mice lacking phosphoinositide 3-kinase p85{alpha}

Amber C. Donahue, Kristen L. Hess, Kwan L. Ng and David A. Fruman

Center for Immunology and Department of Molecular Biology and Biochemistry, University of California, Irvine, CA, USA

Correspondence to: D. Fruman; E-mail: dfruman{at}uci.edu

The signaling enzyme phosphoinositide 3-kinase (PI3K) is activated following B cell receptor (BCR) engagement and by many other receptors on B lymphocytes. Mice lacking p85{alpha}, the predominant PI3K regulatory isoform, exhibit defects in B cell development and activation that are grossly similar to those found in mice lacking Bruton's tyrosine kinase (Btk) and other critical signaling molecules. However, a detailed analysis of splenic B cell subsets in p85{alpha}-deficient mice has not been reported. Here we show that these mice are deficient in four major B cell subsets: transitional-1, transitional-2, follicular and marginal zone. These defects are distinct from those observed in Xid mice that express a mutant Btk unable to interact with PI3K lipid products. Moreover, mice with both genetic lesions exhibit even greater impairment in B cell development. Finally, we show that transgenic expression of the anti-apoptotic protein Bcl-2 in p85{alpha}-deficient mice restores the transitional B cell subsets but not the marginal zone subset, and produces a follicular population with an aberrant phenotype. These findings establish a role for PI3K-p85{alpha} in differentiation of both follicular and marginal zone B cells, and suggest that these functions are required not solely for the propagation of anti-apoptotic signals.

Keywords: B lymphocytes, cellular differentiation, signal transduction, spleen, transgenic/knockout

Transmitting editor: T. Kurosaki


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